Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
Pulmonary edema (PE) is a swelling and/or fluid accumulation in the lungs often caused by heart failure. Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs, particularly pulmonary venous pressure. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs (i.e. the alveoli). This can cause severe respiratory problems and, left untreated, can be fatal. PE can also arise due to other factors besides heart failure, such as infections.
In view of the potential severity of PE, it is highly desirable to detect the condition so that appropriate therapy can be provided. Many patients susceptible to PE are candidates for pacemakers, ICDs, CRT devices or CRT-D devices. A CRT-D is a cardiac resynchronization therapy device with defibrillation capability. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering appropriate pacing stimulus to both ventricles. The stimulus can be synchronized or otherwise controlled so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias.
CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis, et al., entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer, et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann, et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing”. See, also, U.S. Pat. No. 7,065,400 of Schechter, entitled “Method and Apparatus for Automatically Programming CRT Devices”; U.S. Pat. No. 7,010,347 of Schechter, entitled “Optimization of Impedance Signals for Closed Loop Programming of Cardiac Resynchronization Therapy Devices”; U.S. Patent Application No. 2008/0306567 of Park et al., entitled “System and Method for Improving CRT Response and Identifying Potential Non-Responders to CRT Therapy”; and U.S. Patent Application No. 2007/0179390 of Schecter, entitled “Global Cardiac Performance.”
Accordingly, it is desirable to provide such devices with the capability to automatically detect and respond to PE. Aspects of the present invention are primarily directed to this end.
One technique for detecting PE uses transthoracic electrical impedance signals measured using leads of the device to detect a pulmonary “fluid overload,” i.e. a significant increase in pulmonary fluids. In this regard, a significant drop in transthoracic impedance is deemed to be indicative of such a fluid overload. In response, diuretics such as furosemide or bumetanide can be administered to the patient to reduce the fluid overload. (Diuretics are drugs that increase the flow of urine, thus eliminating water from the body, ultimately reducing pulmonary fluid levels.)
The use of impedance is promising since transthoracic impedance can be readily measured in situ using pacemakers, ICDs, CRTs, or CRT-Ds and their leads. However, a significant concern with impedance-based techniques is that such techniques typically cannot be used during an initial lead maturation interval following lead/device implant (also referred to as a lead stabilization phase.) Briefly, to detect PE using transthoracic impedance, as well as to provide for routine cardiac pacing/sensing functions, a set of leads is implanted in the heart. Each lead includes one or more electrodes. Impedance pulses are delivered between the electrodes and the device housing through at least a portion of lung tissue to measure impedance values representative of the amount of fluid within the lungs.
However, during a lead maturation period of about one month following lead implant, the impedance values detected using the leads are deemed to be unreliable because of transient changes in tissues adjacent the leads. For example, fibrous tissue often grows in and around the area of implantation, which can affect the impedance values measured using the leads. As such, impedance measurements made by the implanted device can vary over time as tissue growth occurs, resulting in changes in impedance not due to changes in actual fluid levels.
Typically, therefore, impedance-based PE detection techniques are not activated until completion of a waiting period that is at least as long as the lead maturation period. (The waiting period is typically about two weeks longer than the lead maturation period to permit the device to collect sufficient impedance data following lead maturation to make a reliable detection of PE. That is, the waiting period is typically at least six weeks.) Moreover, with many predecessor techniques, no impedance data is even collected during the initial lead maturation period, i.e. the data is “blanked.”
However, it has been found that heart failure exacerbation events (which trigger episodes of PE) can occur during the waiting period. Hence, it would be highly desirable to provide improved techniques to permit transthoracic impedance to be reliably detected during the waiting period and the present invention is primarily directed to this end.